Serological responses to prednisolone treatment in leprosy reactions: study of TNF-α, antibodies to phenolic glycolipid-1, lipoarabinomanan, ceramide and S100-B
1 CODEWEL Nireekshana ACET India, Narayanaguda, Hyderabad 500029 AP, India
2 Department of Microbiology, Government Institute of Science, Madame Cama Road, Mumbai, India
3 London School of Hygiene & Tropical Medicine, London, UK
4 Department of Neurology and Clinical Neurophysiology, St. Elisabeth Hospital, Tilburg, The Netherlands
5 The Leprosy Mission Hospital, Naini, Allahabad, UP, India
6 Miraj Civil Hospital, Miraj, Maharashtra, India
7 Blue Peter Public Health & Research Centre (BPHRC), Hyderabad, AP, India
8 Mahavir Medical Research Center, 37/165, BhagwanMahavir Marg, AC Guards, Masab Tank, Hyderabad, AP, India
9 The Leprosy Mission Hospital, Faizabad, UP, India
10 Leprosy Unit, Royal Tropical Institute, Amsterdam, The Netherlands
Lipids in Health and Disease 2014, 13:119 doi:10.1186/1476-511X-13-119Published: 28 July 2014
Corticosteroids have been extensively used in the treatment of immunological reactions and neuritis in leprosy. The present study evaluates the serological response to steroid treatment in leprosy reactions and neuritis.
Seven serological markers [TNF-α, antibodies to Phenolic glycolipid-1 (PGL-1 IgM and IgG), Lipoarabinomannan (LAM IgG1 and IgG3), C2-Ceramide and S100 B] were analyzed longitudinally in 72 leprosy patients before, during and after the reaction. At the onset of reaction these patients received a standard course of prednisolone. The levels of the above markers were measured by Enzyme linked immunosorbent assay (ELISA) and compared with the individuals own value in the month prior to the reaction and presented as percentage increase.
One month before the reaction individuals showed a varying increase in the level of different markers such as TNF-α (53%) and antibodies to Ceramide (53%), followed by to PGL-1 (51%), S100B (50%) and LAM (26%). The increase was significantly associated with clinical finding of nerve pain, tenderness and new nerve function impairment. After one month prednisolone therapy, there was a fall in the levels [TNF-α (60%), C2-Ceramide (54%), S100B (67%), PGL-1(47%) and LAM (52%)] with each marker responding differently to steroid.
Reactions in leprosy are inflammatory processes wherein a rise in set of serological markers can be detected a month before the clinical onset of reaction, some of which remain elevated during their action and steroid treatment induces a variable fall in the levels, and this forms the basis for a variable individual response to steroid therapy.